Chronic Obstructive Pulmonary Disease (COPD): History, Examination, Investigations, Treatment

 Chronic Obstructive Pulmonary Disease (COPD)

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow limitation due to impedance to expiratory airflow, mucosal oedema, infection, bronchospasm and bronchoconstriction due to decrease lung elasticity. Smoking is the main cause, but other are chronic asthma, alpha-1 antitrypsin deficiency and chronic infection (e.g. bronchiectasis). 

History 

Exertional dyspnoea, cough, and sputum are usual complaints. Ask about: 

• Present treatment including inhalers, steroids, antibiotics, theophyllines, nebulizers, opiate analgesia, and home O2 treatment. 
• Past history: enquire about previous admissions and co-morbidity. 
• Exercise tolerance: how far can they walk on the flat without stopping ? How many stairs can they climb? Do they get out of the house? .
• Recent history: ask about wheeze and dyspnea,  sputum volume and colour. Chest injuries, abdominal problems and other infections may cause respiratory decompensation. 
• Read the hospital notes: have there been prior ICU assessments? Has the respiratory consultant advised whether ICU would be appropriate? 

Examination 

Examine for dyspnea, tachypnoea, accessory muscle use, and lip-pursing. Look for hyperinflation ( barrel chest ) and listen for wheeze or coarse crackles ( large airway secretions). Cyanosis, plethora (due to secondary polycythemia ) and right heart failure ( cor pulmonale) suggest advanced disease. Look for evidence of hypercarbia: tremor, bounding pulses, peripheral vasodilatation, drowsiness, or confusion. 

Check for evidence of other causes of acute dyspnoea, particularly: asthma, pulmonary oedema, pneumthorax, PE,  Remember that these conditions may co-exist with COPD .

Investigations

• SpO2,  respiratory rate, pulse rate, BP and peak flow if possible. 
• CXR ( look for pneumthorax, hyperinflation, bullae, and pneumonia).
• ECG.
• ABG.(or capillary blood gas),  documenting the FiO2 Use pCO2 to guide O2 therapy.
•  FBC, U&E, glucose, theophylline levels and if pneumonia is suspected and/ or pyrexial, blood cultures, CRP, and pneumococcal antigen. 
• Send sputum for microscopy and culture if purulent. 

Treatment 

Give O2 remember that hypercapnoea with O2 is multifactorial. The aim is to maintain SpO2 88-92% without precipitating  respiratory acidosis or worsening hypercapnoea. If the patient is known to have COPD  and is drowsy or has a documented history of previous hypercapnoeic respiratory failure, give FiO2  of 28% via a Venturi mask  and obtain ABG. Titrate up the FiO2 with serial ABG sampling until the minimum FiO2 that achieves SpO2 88-92% Reduce inhaled oxygen concentration if SpO2 >92%.

Give bronchodilators and steroids 

• Give nebulized salbutamol 5mg or terbutaline 5-10mg
• Consider adding nebulized ipratropium 0.5mg.
• Use O2 driven nebulizers unless the patient has hypercapnoeic, acidotic COPD, in which case use nebulizers driven by compressed air, supplemented by O2 via nasal prongs at 1-4L/min.
• Give steroids (e.g. prednisolone 30mg PO stat or IV hydrocortisone 100mg)

Other drug treatment 

• Give antibiotics ( e.g.amoxicillin, tetracycline or clarithromycin) if the patient reports increased purulent sputum, or there is clinical evidence of pneumonia and/or consolidation on CXR.
• Consider IV aminophylline or salbutamol if there is an inadequate response to nebulized bronchodilators.
• Consider naloxone if the patients is taking an opioid analgesic that may cause respiratory depression. 

Non-invasive ventilation (NIV)

NIV is recommended as standard therapy for hypercapnoeic ventilatory failure during exacerbations of COPD. NIV will improve the blood gas measurement in the ED,  ↓intubation rates, ↓mortality, and length of hospital stay.

NIV takes two forms  CPAP and BiPAP, ( which may be more suitable for treating type II respiratory failure in COPD). Both CPAP and BiPAP  have been used to treat acute cardiogenic pulmonary oedema. Patients with sleep apnoea use CPAP at night. The positive airway pressure is delivered by a tightly adhered face mask, which is sized to fit the patient. The patient is awake, and must be compliant with wearing the mask.

Unlike tracheal intubation, NIV does not protect the airway. Therefore, contraindications include coma vomiting. Absolute contraindications include apnoea and cardiac arrest. A pneumothorax will be converted into a tension pneuomthorax with NIV. Severe agitation may make effective NIV impossible. 

The patient should always be cared for by staff who are familiar with the ventilator and mask, in the resuscitation room.

Start BiPAP at 10cmH2O inspiratory positive airway pressure (IPAP) 5 cmH2O expiratory positive airway pressure (EPAP), and titrate upwards.

• To treat persistent hypercapnoea, increase IPAP by 2cm at a time.
• To treat persistent hypoxia, increase IPAP and EPAP by 2cm at a time 
• The maximum IPAP/EPAP is 25/15cmH2O.
• For CPAP, commence treatment at 5-8 cmH2O